A popular idea suggests a link between big brains and a rich social life, but octopuses don’t fit the pattern, which suggests something else is going on
Scientists have used a NASA-grade supercomputer to push our planet to its limits, virtually fast‑forwarding the clock until complex organisms can no longer survive. The result is a hard upper bound on how long Earth can sustain breathable air and liquid oceans, and it is far less about sudden catastrophe than a slow suffocation driven by the Sun itself. The work turns a hazy, far‑future question into a specific timeline for the end of life as we know it.
Instead of fireballs or rogue asteroids, the simulations point to a world that quietly runs out of oxygen, with only hardy microbes clinging on before even they disappear. It is a stark reminder that Earth’s habitability is not permanent, yet it also stretches over such vast spans of time that our immediate crises still depend on choices made this century, not on the Sun’s distant evolution.
The new modeling effort starts from a simple premise: if I know how the Sun brightens over time and how Earth’s atmosphere responds, I can calculate when conditions for complex life finally fail. Researchers fed a high‑performance system with detailed physics of the atmosphere, oceans and carbon cycle, then let it run through hundreds of thousands of scenarios until the planet’s chemistry tipped past a critical point. One study describes a supercomputer simulation that projects life on Earth ending in roughly 1 billion years, once rising solar heat strips away most atmospheric oxygen.
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A new chip aims to dramatically reduce energy consumption while accelerating the processing of large amounts of data.
A paper on this work appears in the journal Nature Electronics.
The chip was developed by a group of researchers from the Department of Electronics, Information and Bioengineering–DEIB at the Politecnico di Milano, led by Professor Daniele Ielmini, with researcher Piergiulio Mannocci as the first author.
A multidisciplinary team has developed a selective compound that inhibits an enzyme tied to inflammation in people at genetic risk for Alzheimer’s, while preserving normal brain function and crossing the blood-brain barrier.
The findings are published in the journal npj Drug Discovery.
The driver is an enzyme called calcium-dependent phospholipase A2 (cPLA2). The team discovered its role in brain inflammation by studying people who carry the APOE4 gene —the strongest genetic risk factor for Alzheimer’s disease. While many people who have the APOE4 gene don’t develop the disease, those with elevated levels of cPLA2 generally do.
At first glance, some scientific research can seem, well, impractical. When physicists began exploring the strange, subatomic world of quantum mechanics a century ago, they weren’t trying to build better medical tools or high-speed internet. They were simply curious about how the universe worked at its most fundamental level.
Yet without that “curiosity-driven” research—often called basic science—the modern world would look unrecognizable.
“Basic science drives the really big discoveries,” says Steve Kahn, UC Berkeley’s dean of mathematical and physical sciences. “Those paradigm changes are what really drive innovation.”
(Cell Reports 42, 112185; March 28, 2023)
In our article published on March 28, 2023, the representative image for the cGAMP-treated group was inadvertently replaced with that of the control group in STING-KO cells in Figure 7A, resulting in two control panels being displayed. Similarly, the representative image of the control group of WT cells was inadvertently replaced with that of STING-KO cells in Figure S8A, resulting in two control panels of STING-KO cells being displayed. The errors occurred during figure preparation. The authors have carefully re-examined the original data and now provide the corrected version of the figure panels, which accurately present the appropriate control and treated groups.
The errors and their corrections do not affect any of the conclusions reported in the original manuscript. The authors sincerely apologize for any confusion or inconvenience these errors may have caused.
In a historic first for the laboratory, CERN has received $1 billion in private donations to support the development of the Future Circular Collider (FCC).
This philanthropic backing marks a shift in CERN’s 72-year funding history as it seeks to bridge the gap for the project’s estimated $18 billion price tag.
It comes from the Breakthrough Prize Foundation, the Eric and Wendy Schmidt Fund, and billionaire entrepreneurs John Elkann and Xavier Niel. Together, they pledged a combined $1 billion in late December 2025 to jumpstart the project.